This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The C. elegans nematode worm is a very short-living multicellular organism with a lifespan of only 2-3 weeks in optimal laboratory conditions. Such a short lifespan, in addition to accumulated wealth of knowledge about the physiology, morphology and genetics of this organism makes it one of the most convenient models to study the fundamental mechanisms of aging. It has been shown that the lifespan of wild-type C. elegans can be extended drastically in a number of seemingly independent ways. For example it can be extended up to several fold by dietary restriction, by mutation of the Ins/IGF signaling pathway, or by down-regulation of mitochondrial function. Nonetheless, despite the accumulated physiological and primarily genetic data, the molecular mechanisms behind the aging phenomenon and lifespan extension have not been fully outlined yet. In this NCRR collaborative proposal we want to move beyond approaches that have been traditionally used for studying C. elegans aging and take a detailed look at the proteome. Here, in a pilot study, we propose to look at the proteome changes over the age for normally lived worms, long-lived mutant worms and dietary restricted worms. Our goal is to find common downstream proteins or common imprints of certain processes (like specific protein degradation pathways) affecting longevity. This new alternative look at the C. elegans aging process from a proteomics perspective may yield new routes for future research that are not biased by existing aging hypotheses.